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Monitoring of thyroid, liver and pulmonary function tests in patients on amiodarone is less than ideal. This is probably because of lack of awareness of current guidelines.
High levels of RV pacing are associated with heart failure hospitalization and mortality in a large ICD population. However, ICD patients with some RV pacing (10%-19%) exhibit lower event rates compared with those with very low levels (0-9%), possibly due to the physiologically appropriate nature of that RV pacing.
Atrial fibrillations in vivo and in vitro were induced by arrhythmogenic drugs. Action potentials were measured by the standard microelectrode technique.
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Amiodarone-associated thyrotoxicosis (AAT) is often poorly tolerated owing to underlying cardiac disease, and it is frequently refractory to conventional medical treatment. The goal of this study was to describe the patient characteristics, management, and outcomes of all the patients treated surgically for AAT at a single institution. We conducted a retrospective chart review of all patients managed surgically for AAT (April 1985 through November 2002) at the Mayo Clinic in Rochester, Minnesota. Altogether, 29 men and 5 women, ages 39 to 85 years (median 60 years), treated with amiodarone for 3 to 108 months underwent near-total or total thyroidectomy. Frequent symptoms were worsening heart failure, fatigue, weight loss, and tremor. Altogether, 12 patients failed medical management of their AAT, and 21 received no preoperative medical therapy. One patient had been successfully managed medically but required definitive treatment. Common indications for operation were the need to remain on amiodarone, cardiac decompensation, medically refractory disease, and severe symptoms, both hyperthyroid and cardiac, necessitating prompt resolution. The median+/-SD American Society of Anesthesiologists (ASA) classification (1 = healthy through 5 = moribund) was 3.00+/-0.58. A total of 27 specimens had histology consistent with AAT. Complications included death (n = 3), rehospitalization (n = 3), symptomatic hypocalcemia (n = 2), pneumonia (n = 2), cervical hematoma (n = 1), prolonged ventilatorywean (n = 1), and stroke (n = 1); one patient developed hypotension, adult respiratory distress syndrome, and sepsis. Of the 31 surviving patients, 25 (80%) remained on amiodarone postoperatively. The median follow-up was 29 months, at which time all surviving patients were free of hyperthyroid symptoms. Thyroidectomy is an effective treatment for AAT but has a high incidence of perioperative morbidity and mortality. The cardiovascular co-morbidities and high operative risk in this group of patients may account for the increased complication rate.
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Serum Tg-Abs were not elevated in any of the studied groups. However, there were significant differences between A and B and also D and other groups (p<0.05). TPO-Abs titers were not elevated in most cases, there were no significant differences between groups. The serum titers of TSHR-Abs were not elevated in any group. We found statistically significant differences between B and D, C and other groups (p<0.05).
A 22-year-old female, asymptomatic and without any evidence of cardiac disease, was found to have a persistent idioventricular tachycardia (IVT). Sinus rhythm and IVT rates were similar and showed parallel changes in successive resting electrocardiograms. Both IVT and sinus rhythm were transiently slowed or suppressed by vagal stimulation and accelerated by sympathetic stimulation. Long periods of atrial overdrive pacing, at a rate 62% faster than the spontaneous rate of IVT, depressed both ectopic and sinus activity. Fast channel blocking agents (lidocaine, disopyramide), and digoxin and amiodarone failed to modify IVT significantly. Verapamil, a calcium channel blocking drug, allowed total control of the arrhythmia. These electrophysiologic and pharmacologic responses suggest that the IVT may relate to the automatic activity of a ventricular focus of the "slow response" type, functionally resembling an "additional" sinus node with preserved innervation. During an 88-month follow-up, the patient continued to be asymptomatic, warning arrhythmias were never found and the features of IVT remained unmodified.
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Over 300,000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity.A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; beta-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators. Evidence from clinical studies indicates that amiodarone may increase defibrillation threshold (DFT). In addition, some data indicate that drugs including lidocaine, mexiletine, moracizine (moricizine), verapamil, venlafaxine and anaesthetic agents may increase DFT. In contrast, agents including sotalol, dofetilide and beta-adrenergic receptor antagonists (beta-blockers) may reduce DFT. Propafenone and procainamide appear to have minimal effect on DFT. For those antiarrhythmic drugs with both sodium and potassium channel blockade (e.g. amiodarone), the effect of sodium channel blockade predominates, resulting in an increase in DFT. Numerous drugs may affect defibrillation capacity. These effects must be considered when managing patients who have an ICD and require concomitant pharmacotherapy.
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The phosphodiesterase-5 inhibitors (PDE5i) sildenafil, vardenafil, and tadalafil are considered first-line therapy for the treatment of patients with erectile dysfunction (ED). In addition to the classical pro-erectile-effect, clinical findings have suggested that they can also influence vascular tone in pulmonary, coronary and other vascular tissues, as well as improving symptoms associated with benign prostatic hyperplasia. Therefore, considering the hypothetical widespread application of PDE5i, the potential for drug-drug interactions emerges as a relevant factor in determining the safety profile of PDE5i. Review of relevant literature was conducted using data sources from MEDLINE (1998, to June 2007). The use of nitrates remains the only contraindication for all 3 PDE5i. Vardenafil is also not recommended in patients taking type 1A (such as quinidine, or procainamide) or type 3 antiarrhythmics (such as sotalol, or amiodarone) while no other major limitations have been reported for tadalafil and sildenafil. In contrast to previously reported labeling, recent studies have suggested only a precaution, but not contraindication with the concomitant use of alpha-blockers agents. In addition, precaution is also suggested in the presence of potent CYP3A inhibitors, such as azole antifungals, antiretroviral protease inhibitors, or macrolid antibiotics. This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. On the other hand, statins and testosterone seem to have synergic effects with PDE5i on sexual activity.
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Although the clinical features and onset times vary, amiodarone neuromuscular toxicity manifests as a mixed polyneuropathy, vacuolar myopathy, or both. Creatine kinase levels may not correlate with the degree of myopathy. Variable numbers of lysosomal inclusions in peripheral nerve, endothelial cells, and muscle are characteristic.
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The use of IB in patients receiving amiodarone or propafenone for AFL or AF is equally effective and safe as the use of IB alone. The presence of AFL is the stronger predictor factor for cardioversion.
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Amiodarone has been reported to be a remarkably safe and effective drug in the European and South American experience but American investigators have published conflicting data. Since this disparity may be explained by a different dosing schedule, we prospectively evaluated the safety and efficacy of a low dose regimen in a group of 68 patients with cardiac arrhythmia resistant to conventional therapy, of whom 57 had manifested either ventricular tachycardia or fibrillation. All were loaded either intravenously (17) or orally, and maintained on an oral dose of 200 to 600 mg/day (mean daily dose 317 +/- 114 mg) and followed for 4 to 58 months (22 +/- 11). Results indicated that amiodarone was a safe and effective antiarrhythmic drug when used in lower doses.
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In this study, 37 patients with mean ejection fraction (EF%) of 26.2 (8.2) were included. Myocardial performance was assessed by echocardiography and cardiopulmonary exercise testing. Total tri-iodothyronine (T3), thyroxine, and TSH levels were measured in plasma.
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Persistent atrial fibrillation (AF) is characterized by electrical remodeling, ie, marked decreases in the atrial effective refractory period (ERP), ERP rate adaptation, and atrial conduction velocity. Little information is available on the effects of class III antiarrhythmic drugs on the remodeled atrium. We studied the effects of the class III antiarrhythmic drugs nifekalant, ibutilide, and amiodarone on rate-dependent changes in atrial action potential duration in patients with persistent AF. Right atrial (RA) monophasic action potential duration (MAPD) and intra-atrial conduction time (IACT) were measured at pacing cycle lengths (CLs) of 800, 700, 600, 500, 400, 350, 300, and 250 ms before and after administration of nifekalant (0.4 mg/kg + 0.3 mg/kg/hr, iv), amiodarone (5 mg/kg, iv), or ibutilide (0.01 mg/kg, iv) in 31 patients after successful internal cardioversion of chronic AF of > 2 months duration. Nifekalant and ibutilide significantly increased RA MAPD and the ERP at each CL in a reverse rate-dependent manner. Amiodarone did not affect RA MAPD. Nifekalant did not affect IACT, whereas amiodarone increased IACT at each CL in a rate-dependent manner, and ibutilide increased IACT at CLs ≤ 350 ms. The atrial electrophysiologic effects of the class III antiarrhythmic drugs nifekalant, amiodarone, and ibutilide differ, depending on the degree of electrical and structural remodeling and the effects of the drugs on the depolarizing and repolarizing currents.
To describe the treatment of persistent supraventricular tachycardia (SVT) in a young horse in endurance training.
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Amiodarone, an efficacious and widely used antiarrhythmic agent, has been reported to cause hepatotoxicity in some patients. To gain insight into the mechanism of this unwanted effect, mice were administered various doses of amiodarone and examined for changes in hepatic histology and gene regulation. Amiodarone induced hepatomegaly, hepatocyte microvesicular lipid accumulation, and a significant decrease in serum triglycerides and glucose. Northern blot analysis of hepatic RNA revealed a dose-dependent increase in the expression of a number of genes critical for fatty acid oxidation, lipoprotein assembly, and lipid transport. Many of these genes are regulated by the peroxisome proliferator-activated receptor-alpha (PPARalpha), a ligand-activated nuclear hormone receptor transcription factor. The absence of induction of these genes as well as hepatomegaly in PPARalpha knockout [PPARalpha-/-] mice indicated that the effects of amiodarone were dependent upon the presence of a functional PPARalpha gene. Compared to wild-type mice, treatment of PPARalpha-/- mice with amiodarone resulted in an increased rate and extent of total body weight loss. The inability of amiodarone to directly activate either human or mouse PPARalpha transiently expressed in human HepG2 hepatoma cells indicates that the effects of amiodarone on the function of this receptor were indirect. Based upon these results, we conclude that amiodarone disrupts hepatic lipid homeostasis and that the increased expression of PPARalpha target genes is secondary to this toxic effect. These results provide important new mechanistic information regarding the hepatotoxic effects of amiodarone and indicate that PPARalpha protects against amiodarone-induced hepatotoxicity.
Iodine intake is often measured by a surrogate measure, namely urine iodine excretion as almost all ingested iodine is excreted in the urine. However, the methods for urine collection and the reporting of the results vary. These methods, and their advantages and disadvantages, are considered in this article.
Diabetes mellitus is a risk factor for coronarosclerosis and for high mortality after myocardial infarction (MI). The causes of this high mortality are: more extensive and premature coronarosclerosis, more frequent left ventricular dysfunction, worse glycemic control with increased myocardial oxygen consumption, sulfanylurea drugs before and during MI. The results of a multicenter study (DIGAMI) and other studies suggest that a better control of diabetes using intravenous infusion of insulin and glucose, followed by long-term (3 months) intensive insulin therapy subcutaneously, improves long-term prognosis after MI. The relative reduction of mortality at the end of follow-up (3.4 years) is 28%. Thrombolysis reduces mainly mortality in hospital,s period and does not provoke retinal haemorrhages. Aspirin lowers the relative risk of mortality to 0.72. The beta-blockers are less used in diabetic patients because they probably alter diabetic control, lipid profile and "mask" the hypoglycemic symptoms, but the results of the beta-blocker's effect concerning reduction of mortality are convincing. ACE inhibitors and statins also reduce mortality in diabetics with MI, via beneficial influence of endothelial dysfunction. The ATMA study registers reduction of rhythmogenic mortality by 29% with amiodarone in high risk of arrhythmia after MI. The invasive methods of treatment in diabetes are accompanied by higher risk of reobstruction. The attempt to reduce this tendency is realizable with intracoronary stents, glycoprotein IIb/IIIa inhibitors and aggressive early treatment of all other risk factors.
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Dronedarone is an amiodarone derivative that was approved in the US in July 2009 to reduce the risk of cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF), who are in sinus rhythm (SR), or who will be cardioverted.
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Hyperkalemia is a potentially life-threatening disorder frequently occurring in hospitalized patients. The ischemic myocardium releases potassium into the extracellular space which can cause regional hyperkalemia. These changes may modify the effects of anti-arrhythmic drugs acting on the rapid component of the delayed rectifier potassium current (IKr). We evaluated the influence of increased extracellular potassium concentration [K(+)](e) on IKr inhibition by amiodarone, azimilide, dofetilide, quinidine and sotalol.
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Spontaneous reports in the United States Food and Drug Administration (FDA) Adverse Event Reporting System (AERS) database generated between July 1, 2009, and June 30, 2011.
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Consecutive AIT patients (n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006.
Ventricular tachycardia (VT) is found usually in patients with structural heart disease. Its symptomatology depends on haemodynamic manifestations. ECG criteria for the diagnosis of VT are known. For the classification of VT we use morphological criteria (monomorphous and polymorphous), duration of arrhythmia (non-and sustained VT) and the pathomechanism of VT (re-entry, increased automation and triggered activity). The clinical impact of VT and the therapeutic approach depend to a great extent on the basic disease. The therapeutic results and prognostic estimates assembled in ischaemic heart disease cannot be mechanically applied in non-ischaemic heart disease. The authors mention the prevalence of VT and the approach to its treatment in dilatative cardiomyopathy, in prolapse of the mitral valve, in hypertrophic cardiomyopathy, in arrhythmogenic right ventricular dysplasia and in patients with a "normal" heart. Only collection of the necessary data and their analysis will help us to achieve better therapeutic results. In the treatment authors focus attention first of all on the pharmacological approach. They emphasize the need of thorough and comprehensive examination of the patient, draw attention to proarrhythmia. In the prevention of relapses of VT most frequently beta-blockers and amiodarone are used (either alone or combined).
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Central cannulation in the fibrinolytic state is associated with a low incidence of important bleeding complications. Thrombolysis should not be withheld in these patients. Cannulation via the subclavian route, however, should be avoided in patients undergoing thrombolysis.
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Cardioversion followed by low-dose amiodarone to maintain normal sinus rhythm appears to be a relatively safe and effective treatment for patients with chronic atrial fibrillation.
Dronedarone, a multiple ion channel blocker is prescribed for the treatment of paroxysmal and persistent atrial fibrillation. While dronedarone does not precipitate toxicities like its predecessor amiodarone, its clinical use has been associated with idiosyncratic hepatic and cardiac adverse effects and drug-drug interactions (DDIs). As dronedarone is a potent mechanism-based inactivator of CYP3A4 and CYP3A5, a question arose if it exerts a similar inhibitory effect on CYP2J2, a prominent cardiac CYP450 enzyme. In this study, we demonstrated that CYP2J2 is reversibly inhibited by dronedarone (Ki=0.034 μM), amiodarone (Ki=4.8μM) and their respective pharmacologically active metabolites namely N-desbutyldronedarone (NDBD) (Ki=0.55 μM) and N-desethylamiodarone (NDEA) (Ki=7.4 μM). Moreover, time-, concentration- and NADPH-dependent irreversible inactivation of CYP2J2 was investigated where inactivation kinetic parameters (KI, kinact) and partition ratio (r) of dronedarone (0.05 μM, 0.034 min(-1), 3.3), amiodarone (0.21 μM, 0.015 min(-1), 20.7) and NDBD (0.48 μM, 0.024 min(-1), 21.7) were observed except for NDEA. The absence of the characteristic Soret peak, lack of recovery of CYP2J2 activity upon dialysis, and biotransformation of dronedarone and NDBD to quinone-oxime reactive metabolites further confirmed the irreversible inactivation of CYP2J2 by dronedarone and NDBD is via the covalent adduction of CYP2J2. Our novel findings illuminate the possible mechanisms of DDIs and cardiac adverse effects due to both reversible inhibition and irreversible inactivation of CYP2J2 by dronedarone, amiodarone and their active metabolites.
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This is a prospective study of 132 patients, without previous thyroid dysfunction, chronically treated with amiodarone for cardiac arrhythmias, to determine the incidence of thyroid dysfunction. Age was 62 +/- 11 years (mean +/- SD); 54 were female and 78 male. The arrhythmia was supraventricular in 66%, ventricular in 26.5%, and both in 7.5%. Amiodarone dose was 2,390 +/- 65 mg/week, and follow-up 20 +/- 9 months (minimum 9 months). Thyroid status was evaluated at the onset and at regular intervals during follow-up by means of clinical indexes defined by Crooks et al and Billewicz et al. During follow-up 4 patients developed diagnostic indexes (two hyperthyroid and two hypothyroid) and seven more developed suggestive symptoms without reaching a diagnostic index. Biochemical serum determinations of thyroid function proved dysfunction in the four with diagnostic indexes, and were normal in the other seven. The prevalence of new thyroid dysfunction in patients chronically treated with amiodarone in our population is 3%, with equal incidence of hyper and hypofunction. This is the expected incidence for an area with adequate dietary iodine intake. The use of clinical indexes of thyroid dysfunction appear as a useful and economical means of following thyroid function in these patients, saving a large number of biochemical tests.
Because of the inducible and prolonged VT, despite antiarrhythmic treatment with amiodarone, a cardioverter-defibrillator was implanted (ICD). During threshold measurements of the pacemaker integrated into the ICD the pacemaker impulse was noted to produce a right bundle branch block pattern, the ICD lead having erroneously been placed in the left ventricle via a patent foramen ovale. The lead was left in place, because the ICD was functioning well and lead removal with the possible need of a thoracotomy carried a high risk.
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Although amiodarone is one of the most effective pharmacologic agents used in clinical management of atrial fibrillation (AF), little is known about its differential effects in atrial and ventricular myocardium.